Male Reproductive Disorders

PHIMOSIS
 Phimosis
 A state in which the male foreskin is
unable to retract properly from the head of
the penis (glans). This is due to an
unusual tight foreskin
 It is not painful, but it can lead to
obstructive uropathy if it is severe enough.
Type of Phimosis

A. Infantile or
congenital

Infants are
born with
phimosis
Type of Phimosis
B. Acquired (adult)

result of repeated
foreskin infections
such as balanitis.

also linked with

neglected hygiene.
 ETIOLOGY
 Result of inflammation or local trauma.

 Uncircumcised adult male

 Congenital
Phimosis Pathophysiology
 Uncleaned Preputial

Normal Secretion

Balanitis Secretions Thickened

Adhesion Encrusted w/ urinary salts & calcify

Fibrosis Forming calculi in prepuce

Interfere with urinary elimination and intercourse

Malignant changes of the penis

 Complications
 Painful erection
 Difficulty in urinating
 Balanitis – inflammation of the penis head
 Frequent and recurrent infections under the
foreskin
 Paraphimosis
 is a condition where there is constriction in

the glans penis by a foreskin

 Nursing Diagnosis
1. Self-Esteem Disturbance r/t negative
feeling of himself due to his illness.
2. Knowledge Deficit (Specify) r/t
unfamiliarity of condition.
3. Altered Urinary Elimination r/t congenital
adhesion of glans penis.
4. Altered Sexual Function r/t recurrent
penile infection.
 Diagnosis
Physical examination
 Palpate the penis, scrotum, prostate gland, and
rectum.
 Inspect the penis for lesions, swelling,
inflammation, scars, or discharge.
 In the uncircumcised male, retract the foreskin to
visualize the glans.
 Examine the scrotum for size, shape, and
abnormalities, such as nodules or inflammation.
 Check for the presence of both testes
HYPOSPADIAS
 Hypospadia

Developmental anomaly
in which the male urethra
opens on the underside of
the penis.

The opening can occur

anywhere from just below
the end of the penis to the
scrotum.
One distinguishes various
anatomic variants
One distinguishes various
anatomic variants
 Etiology
Genetic factors
 A genetic predisposition has been suggested by

the 8-fold increase in incidence of hypospadias

among monozygotic twins compared with
singletons.
 Familial trend with hypospadias

Endocrine factors
 A decrease in available androgen or an inability to

use available androgen.

 Endocrinopathies or fetal endocrine

abnormalities.
 Etiology
Environmental factors
 Environmental substances with significant

estrogenic activity are ubiquitous in

industrialized society and are ingested as
pesticides on fruits and vegetables,
endogenous plant estrogens, in milk from
lactating pregnant dairy cows.

 An increase in estradiol concentration in

placental basal syncytiotrophoblasts of
boys with undescended testes compared
with a control population.
EPISPADIAS
 Epispadias
Birth defect due to malformation of the
URETHRA in which the urethral opening
is above its normal location.

 In male, the malformed urethra opens

on the top or the side of the PENIS.
 In female, the malformed urethral
opening is often between the CLITORIS
and the labia, or in the ABDOMEN."
Type of Epispadias

Glandular type

 Affects the distal

part of the urethra.
Type of Epispadias
Penile type

• Entire penile
urethra is affected,
with an external
meatus on the
dorsal shaft of the
penis
Type of Epispadias
Complete or
Penopubic type

• A total deficiency
of the dorsal wall
of the urethra and
the anterior wall
of the bladder is
present
 Etiology 
 Epispadias are unknown at this time.
 Related to improper development of the
pubic associated with bladder extrophy,
 Can also occur alone or with defects.
Manifestations
In males:
 Abnormal opening from the joint between
the pubic bones to the area above the tip of
the penis
 Backward flow of urine into the kidney
(reflux nephropathy)
 Short, widened penis with an abnormal
curvature
 Urinary tract infections
Manifestations
In females:
 Abnormal clitoris and labia

 Abnormal opening where the from the bladder neck to the

area above the normal urethral opening

 Backward flow of urine into the kidney

(reflux nephropathy)
 Urinary incontinence

 Urinary tract infections

 Complications
 Bleeding
 Infection
 Wound separation
 Flap necrosis
 Edema
 Urethrocutaneous fistula with urinary
leakage
 Persistent urinary incontinence
 Upper urinary tract (ureter and kidney)
damage
 Infertility
 Diagnostics
 Intravenous pyelogram (IVP),
- a special x-ray of the kidneys, bladder,
and ureters
 Pelvic x-ray
 UTZ of the urogenital system
 Nursing Diagnosis
1. Body image disturbance r/t alteration in penile
structure.
2. Fear r/t developmental concerns with body
integrity. – patient may experience fear caused
by awareness of pain or danger concerning
body function.
3. Altered pattern of urinary elimination r/t surgical
repair. – patient may experience incontinent of
passing urine due to surgery.
4. High risk for fluid volume deficit r/t post operative
hemorrhage.
 Medical Interventions

Surgical
 Surgical repair of epispadias is
recommended in patients with more than
a mild case. Leakage of urine
(incontinence) is not uncommon and may
require a second operation.
 2. Wide diastasis of the pubic bone 3. Distal epispadias. Outlining of
1.Distal penile
and external displacement of the local flaps from the glans to
epispadias hips in epispadias. reconstruct the distal urethra.

4.Vertical island flap drawn on the

ventral aspect of the penis
9. Final Apperance

8. Drawing of the final

appearance at the end of
the operation.

6. Island flap sutured into 5. Island flap transferred

a tube to reconstruct the dorsally and
7. Urethral reconstruction
missing portion of the anastomosed to the
is completed
urethra urethra.
CRYPTORCHIDISM
 Cryptorchidism
 The absence of one or both testes
from the scrotum.
A testis absent from the normal
scrotal position can be:
 Etiology
 Severely premature infants
 Deficient maternal gonadotropin
stimulation
 Mechanical factor:
 Short spermatic cord
 Adhesions in the normal path of testes.
 Narrowed inguinal canal.
 Complications
 Impaired spermatogenis
- caused by higher temperature in the abdomen.
- Impaird fertility
 ↓ sperm counts
 Testicular cancer (Seminoma)
- higher incidence of neoplastic processes, the risk of testicular Ca is 35-50 times higher with
cryptorchydism.
 Surgical Procedures
 Orchiopexy
 Auto-transplantation
of testis into the
scrotum
Nursing Diagnosis
Mild Anxiety r/t intensive diagnostic and surgical
procedures.
Pain r/t invasive procedure
Risk for infection r/t bacterial invasion
of wound or bladder
Ineffective individual and family coping r/t
infertility and family relationship
Body image disturbance r/t perceived body
image changes
Knowledge deficit r/t new condition
 Diagnostic Tests
Pelvic ultrasound
MRI
Ultrasonography
CT scan
Laparoscopy
Karyotyping
number, form, size, and arrangement of within
the nucleus of the somatic chromosomes of an
individual. as determine by microphotograph
taken during metaphase of mitosis.
Hydrocele
 Hydrocele
Collection of fluid between the
visceral and parietal layers of the
tunica vaginalis of the testicles or
along the spermatic. Most common
form of scrotal swelling
Visceral tunica vaginalis

Parietal tunica vaginalis

 Types Hydrocele

Communicating (Infants)

 Incomplete obliteration
of processus vaginalis

 Open communication
between peritoneum
and tunica
 Closes spontaneously
in the first year of life
 Types Hydrocele
Non-Communicating (Adults)

 Imbalance in secretive
and absorptive capacities
of scrotal tissues.
 Results from inflammatory
reaction
a. injury
b. infection
c. testicular tumor
 Etiology
- Communicating hydrocele
-caused by failed closure of processus
vaginalis.

-Non- communicating hydrocele

-pathologic closure of the processus
vaginalis and trapping of peritoneal fluid.
 Etiology
Adult onset may be caused by secondary
-Infection (epididymytis, Orchitis)
-Local trauma
-Radiation
-Testicular torsion
-Tumor of the testicular adnexa
 Pathophysiology
A communicating hydrocele, a congenital
condition, occurs because of patency between
the scrotal sac and peritoneal cavity, which
allows peritoneal fluids to collect in the scrotum.

Non-communicating hydrocele, fluids

accumulate because of infection, trauma, tumor,
an imbalance between the secreting and
absorptive capacities of scrotal tissue, or an
obstruction of lymphatic or venous drainage in
the spermatic cord.
 Complications
 Testicular atrophy
 Compression of testicular blood supply.
 Ischemia
 Impairment of fertility.
 Hemorrhage
 Testicular trauma
 Incarceration or strangulation of an
associated hernia may occur.
 Epididymitis, Orchitis
Nursing Diagnosis
1. Body Image Disturbance related to increase
size of Hydrocele
2. Alteration in Comfort r/t scrotal enlargement.
3. Risk for infection r/t bacterial invasion of
wound or bladder
4. High Risk for Sexual Dysfunction r/t excision
of tunica vaginalis.
- may lose sexual urges due to surgery.
Cont.. Nursing Diagnosis
5. Impaired skin integrity r/t presence of incision
made during surgery.
6. High risk for infection r/t fluid accumulation
fluid in the scrotum.
- fluid that is collected at the scrotal sac may
cause infection.
7. Mild Anxiety r/t intrusive diagnostic, surgical
test and procedure.
– patient may feel very anxious about the
procedures that will be done to him.
 Radiologic Studies

 Inguinal-scrotal imaging ultrasound

 Doppler ultrasound flow study
 Testicular scintigraphy
 Abdominal x-ray
Varicocele
Overview

Abnormal enlargement of the veins

in the spermatic cord.

Classically described as a
“Bag of worms”
 Etiology
 Incompetent or congenitally absent valves
in the spermatic veins

 Tumor or thrombus obstructing the inferior

vena cava (unilateral [left-sided]
varicocele)
 Idiopathic
 Types of Varicocele
Idiopathic
 valves within the veins
along the spermatic cord
don't work properly.
 results in backflow of blood
into the pampiniform plexus
and causes ↑pressures
 ultimately, leading to
damage to the testicular
tissue.
 Types of Varicocele
Secondary
 due to compression of the
venous drainage of the
testicle, also-called "SMA”

 compresses the left renal

vein, causing ↑pressures
there to be transmitted
retrograde into the left
pampiniform plexus.
Manifestations
 Dragging-like or aching pain within scrotum.
 Feeling of heaviness in the testicle(s)
 Infertility
 Atrophy (shrinking) of the testicle(s)
 Visible or palpable enlarged vein
 Complications after
Surgery
 Hematoma
 Injury to the scrotal tissue or structures
 Infection
 Nursing Diagnosis
 High Risk Sexual Dysfunction r/t injury to
excision of tunica vaginalis
 Pain r/t scrotal compression .
 Impaired Skin Integrity r/t surgical repair of the
scrotum
 High Risk for Infection r/t scrotal fluid
accumulation
 Mild Anxiety r/t intrusive diagnostic surgical test
and procedure.
 Diagnostics
 Physical examination allows palpation of the
“bag of worms” when the patient is upright

 Ultrasonography

 Radioisotope scanning

 Spermatic venography

 Scrotopenography
Surgical Intervention
 Varicocelectomy
 Three most common approaches:
 inguinal (groin),
 retroperitoneal (abdominal)
 infrainguinal/subinguinal (below the groin)
 Embolization
 Surgical ligation
 A 2- to 3-inch incision is made in the groin or
lower abdomen, the affected veins are located
visually, and the surgeon cuts the veins and ties
them off above the varicocele to reroute the
blood through unaffected veins.
 What is BPH?
 Is an enlargement of the prostate
gland cause by hyperplasia (not
hypertrophy) of glandular and cellular
tissue.
 PROSTATE GLAND FUNCTION
Secrete alkaline fluid that forms part of the
seminal fluid that carries sperm
Liquefy and promote sperm motility
Protect sperm from acidic fluids of the male
urethra and female vagina
During climax, prostate muscular glands
help to propel the prostate fluid.
PSA and PSAP are produced in the
epithelial cells.
BPH

Prostate Ca
 Early in puberty- double in size.
Age 25- begins to grow again.
Rapid development that continues until
the 3rd decade.
The prostate continues to grow during most of
a man's life, the enlargement doesn't usually
cause problems until late in life.
 Pathogenesis
Androgen:
-Androgen Receptors are located primarily in
epithelial cells of normal prostate tissue, but in
hyperplastic glands ARs are distributed in
epithelial and stromal cells.

- Men with (5αR) 5-α-Reductase deficiency have

rudimentary prostates throughout life.
- Similar DHT levels in BPH and non BPH.
- DHT is necessary but not sufficient to cause
BPH.
 Pathogenesis
Estrogen:
- Conflicting evidence.
- 86 men between 52 and 82 years of
age, TZ volume correlated with
increasing serum estrone.

Dysregulation of stromal growth factors:

Prostate reverts embryonic state sensitive to
IGF2 and TGFß stimulating growth.
 Pathogenesis
Genetics:-Survey Olmsted County, Minnesota, 21
percent of 2,119 men between 40 and 70 years of age
had a family history of an enlarged prostate (1)

-Case-control study of men under 64 years

of age who had undergone prostatectomy for BPH
and in whom more than 37 grams of tissue was
resected . The first-degree relatives of these men had
a four-fold increased risk of developing BPH that
required surgical therapy as compared with the
relatives of normal men.
Benign Prostatic Hypertrophy (BPH)—
Pathophysiology
 Common in older men; varies from mild to severe
 Change is actually hyperplasia of prostate
 Nodules form around urethra
 Result of imbalance between estrogen and testosterone
 No connection w/ prostate cancer
 Rectal exams reveals enlarged gland
 Incomplete emptying of bladder leads to infections
 Continued obstruction leads to distended bladder, dilated
ureters, renal damage
 If significant, surgery required
 NODULES (hyperplasia and hypertrophy)
FORMS IN THE INNER PROSTATE

URETHRA IS COMPRESSED
Difficulty of
initiating OBSTRUCTION TO FLOW OF URINE
micturation,
dribbling
INCOMPLETE EMPTYING OF BLADDER

↑Frequency INFECTION Bladder distension

Delay (Cystitis)
Decrease force HYDRONEPHROSIS
ASCENDS TO KIDNEYS
(pyelonephritis) KIDNEY DAMAGE
Normal prostate vs. BPH
 BPH—Signs and Symptoms
 Initial signs
 Obstruction of urine flow
• Hesitancy, dribbling, decreased force
of urine stream
• Incomplete bladder emptying
 Frequency, nocturia, recurrent UTIs
 Nursing Diagnosis
 Impaired Urinary Elimination r/t obstruction
by enlarged prostate
 Risk for Deficient Fluid Volume r/t
postoperative bleeding
 Urinary Retention r/t blockage by enlarged
prostate
 2 helpful serum markers
 Prostate-specific Antigen (PSA)
 NV: 0-4 ng/mL
 Useful screening tool for early detection
 Prostatic – specific acid phosphatase
 elevated when metastatic cancer present
 < . 10 consistent with BPH
 > .15 suggest the presence of cancer
 Ultrasound and biopsy confirms
Prostate-Specific Antigen (PSA) Blood Test
- To rule out cancer as a cause of urinary symptoms. PSA, a
protein produced by prostate cells, is frequently present at
elevated levels in the blood of men who have prostate
cancer.
- Men at risk for BPH are also at risk for prostate cancer

PSAD: helpful in differentiating BPH from Prostatic Ca.

____Serum PSA____
Volume of Prostate Tissue
Digital Rectal Examination (DRE)
- The doctor inserts a gloved finger into the rectum
and feels the part of the prostate next to the rectum.

DRE + PSA = are conducted to determine

hyperplasia
Urinalysis

Examine the urine using dipstick methods

and/or via centrifuged sediment evaluation to
assess for the presence of blood, leukocytes,
bacteria, protein, or glucose.

Urine C&S
Female Reproductive
Organ Disorders
Pelvic Relaxation Disorders
Overview
Pelvic relaxation is a progressive and is
related to inherent strength or weakness of
woman’s musculofascial tissue.

Muscular and fascial tissue loses tone and

strength with aging and may fail to
maintain the pelvic organs in the proper
position.
Pelvic Organ Prolapse (POP)
Causes
- Straining (defecation)
-Trauma to fascia and levator ani muscle
-Childbirth (prolonged labor)
-Multiple birth
-Birth of large baby
-Neuromuscular dysfunction
Pathophysiology
-Attenuation of pelvic support structures
 tears or breaks
 neuromuscular dysfunction
 both
 Pelvic support structures

-Endopelvic connective tissue  cardinal uterosacral

ligament complex
- Pelvic diaphragm
- levator ani and coccygeus muscles
- provides basal tonicity and support of the pelvic
structures - when contracted (increased abdominal
pressure), the rectum, vagina and urethra are
pulled anteriorly toward the pubis
Sagital oblique view of the distal midvagina
A saggital view of the female pelvis with bladder and uterus removed (ureters,
trigone, and cervix intact) illustrating anterior and posterior vaginal fibromuscular
planes, their endopelvic fascial attachments, and a functional pelvic floor.

Endopelvic
Connective
tissue

Denonvillier’s fascia
of posterior
vaginal wall
RECTOCELE
-protrusion of the rectum into the vaginal lumen
-weak muscular wall of rectum and paravaginal
connective tissue (holds rectum posteriorly)
View of pelvic cavity with bladder, upper vagina and sigmoid
colon removed

Pararectal
Fascia
Vagina

Rectum
Posterior vaginal musculo-
connective tissue
ENTEROCELE
- herniation of rectouterine pouch into the
rectovaginal septum (bet. rectum and post. vaginal
wall)
- occurs downward (bet. uterosacral ligament and
rectovaginal space)
- apically (previous hysterectomy)
Enterocele
CYSTOCELE
- descent of the bladder and the anterior vaginal
wall into the vaginal canal
- cause by weaknes of pubocervical
musculoconnective tissue at midline or detaches
from its lateral or superior connecting points
- occurs downward (bet. uterosacral ligament and
rectovaginal space)
- apically (previous hysterectomy)
Uterine Prolapse 101
Uterine Prolapse 102
Uterine Prolapse 103
Uterine Prolapse
Definition

Is descent of the cervix or

the entire uterus into the
vaginal canal. In severe
cases the uterus falls
completely through the
vagina and protrude from the
introitus. Usually classified
as one of three degrees.
Uterine Prolapse
Uterine Prolapse
Uterine Prolapse
Causes

1. The stretching of muscle and

fibrous tissue (cardinal,uterosacral
ligaments)
2. Increased intra-abdominal pressure
3. A constitutional predisposition to
stretching of the ligaments as a
response presumably to years in the
erect position
Uterine Prolapse
Uterine Prolapse
• In recent years,the incidence of
prolapse is greatly reduced. The
more liberal use of caesarean
section and the elimination of
labours are probably the two most
important factors.
Risk Factors
Increased intraabdominal pressure
ascites, large pelvic or intraabdominal tumors
Sacral nerve disorders (S1-S4), Diabetic
neuropathy
Chronic respiratory disease
chronic bronchitis, asthma, bronchiectasis
Severe obesity
Congenital
Pathophysiology

Poor cardinal or uterosacral

ligament apical support

Downward protrusion of cervix

and uterus towards the introitus

Prolapse of uterus and

vagina (Procidentia)

EVERSION OF VAGINA
Uterine prolapse with apical detachment from the uterosacral
ligament complex and lateral wall detachment from the
endopelvic connective tissue.
Procedentia of the uterus and vagina
Degrees of uterine prolapse

First degree: cervix still inside vagina

Uterine Prolapse
Degrees of uterine prolapse
• Second degree: the cervix appears outside
the vulva. The cervical lips may become
congested and ulcerated

Uterine Prolapse
Degrees of uterine prolapse

• Third degree: complete prolapse.In the picture the

uterus is retroflexed,and the outline of bladder can be
seen.This is sometimes called complete procidentia.

Uterine Prolapse 121

Symptoms

• Something coming down

• Backache
• Increased frequency of
micturition
• A ‘bearing down’ sensation
• Coital problems
• Difficulty in voiding urine
Symptoms

•Voiding dysfunction (urinary

incontinence)
• urinary urgency and frequency
• urinary retention and upper renal
compromise (pain and anuria)
Symptoms

•Pelvic pain
•Defecatory problems (constipation,

diarrhea, fecal incontinence)

• Overall pelvic discomfort
• Dyspareunia
-Possible complications:

- vaginal discharge and odor

- excoriation and irritation
- stress incontinence
rare: vesicovaginal fistula, small bowel

entrapment, hydronephrosis,
urosepsis
Nursing Diagnosis

1. Mild Anxiety related to change in

health status
2. Disturbed body image related to
protrusion of uterus to the vaginal
opening.
3. Stress urinary incontinence related

to weak pelvic musculature

Diagnosis

• A pelvic examination reveals

protrusion of the cervix into the
lower part of the vagina (mild
prolapse), past the vaginal
introitus/opening (moderate),
or protrusion of the entire uterus
past the vaginal introitus/opening
(severe).
Surgery

* Anterior colporrhaphy
(and repair of cystocele)
* Posterior colpoperineorrhaphy
(including repair of rectocele)
* Manchester repair
* Vaginal hysterectomy
Uterine Prolapse
Uterine Prolapse
Pelvic Muscle Function Assessment
Pt in lithotomy position – bimanual examination

– palpate puborectalis (4 and 8 o’ clock)

basal muscle tone, strength, duration and
symmetry of contraction
Rectovaginal examination
assess basal and contraction muscle tone of the

anal sphincter complex

Imaging
- fluoroscopic evaluation of bladder
function
- pelvic USG
- defecography (intussusception, rectal
mucosal prolapse)
- MRI (pelvic pathology)
Pessary
.
 Leiomyomas
 Benign growth of smooth muscle in
the wall of the uterus. solid tumor
made of fibrous tissue, hence it is
often called a 'fibroid' tumor
 commonly called uterine fibroids.
 vary in size and number, are most
often slow-growing.
Cause

• Unknown
• Related to hormonal
fluctuation (particularly
estrogen)
Risk factors
- Early Menarche
- Obesity
- Lifestyle
- High-fat Diet
- Family history
- Nulliparity
- Use of oral contraceptives
- Anovulation
Locations

INTRAMURAL
SUBMUCOUS

SUBSEROUS
 Leiyomyoma
Pathophysiology
 ↑ Estrogen and Progesterone

promote the growth of fibroids

Develop in smooth muscle tissue in the uterus

Single cell reproduces repeatedly

Creating a pale, firm, rubbery mass distinct

from neighboring tissue

Pain Fibroid enlarges in the uterus

 Fibroid enlarges in the uterus

Vaginal bleeding ulceration

Abdominal pressure develop slowly

Bladder: Ureter:
Urinary frequency, Rectosigmoid: “upstream”
urgency, dysuria Constipation from the
pressure point
Clinical manifestation
• Increase amount and duration of bleeding
(menorrhagia)
• Prolonged menstrual periods or bleeding
between periods (menorrmetrorrhagia)
• Spotting or bleeding between periods
• Pelvic pressure or pain
• Urinary incontinence or frequent urination
• Constipation
• Pain with intercourse
• Difficulty emptying your bladder
• Difficulty moving your bowels
Complications
• Anemia-from heavy blood loss
• distort or block your fallopian tubes
• interfere with the passage of sperm from cervix to fallopian tubes
• may prevent implantation and growth of an embryo
• slightly increased risk of miscarriage
• premature labor and delivery
• abnormal fetal position
• separation of the placenta from the uterine wall
NURSING DIAGNOSIS
• Acute pain r/t stimulation of free nerve ending 2 to enlargement
of tumor.
• Constipation r/t decrease transit time of feces 2 to compression
of large colon.
• Deficient knowledge related to new condition
• Disturbed body image r/t permanent alteration in function of a
body part 2 to removal of uterus.
Diagnostic Tests

 Ultrasound
 Transvaginal
ultrasound
 Hysterosalphingo-
graphy
 Hysteroscopy
 CT scan
 MRI
 Endometriosis
• Presence of functioning endometrial tissue
outside uterus (ectopic)
– Found on ovaries, ligaments, colon, sometimes lungs
• Responds to cyclic hormonal variations
– Grows and secretes then degenerates, sheds and
bleeds
• What is the problem? (Where does it go?)
– Blood irritating to tissues = inflammation and pain
• Recurs w/ every cycle w/ eventual fibrous tissue
– Causes adhesions and obstruction
• Diagnosis confirmed w/ laparoscopy
Pelvic Sites of Endometrial Implantation
 What causes
• Cause not established
– Migration of endometrial tissue up thru tubes to
peritoneal cavity during menstruation, development
from embryonic tissue at other sites, spread thru
blood or lymph, transplantation during surgery (C-
section) all possibilities
 Theories of Endometriosis
• Implantation of endometrial cells during retrograde
menstruation
• Spread of endometrial cells through the vascular or
lymphatic systems
• Immunologic factor that may include depressed
cytotoxic T cells response to endometrial cells.
• Stimulations of multipotent epithelial cells covering
the reproductive organs that develop into the
endometrial cells.
• Genetic predisposition based on familial tendencies.

Clinical gynecology endocrinology and fertility, ed 7 Philadelphia, 2005, Lippimcott Williams

 Manifestations
• Primary manifestations
– Dysmenorrhea
• More severe e/ month
– Painful intercourse if vagina and supporting ligaments
affected by adhesions
• “chocolate cyst” develops on ovary
– Fibrous sac containing old brown blood
• Dyschezia, a hallmark symptom endometriosis.
– occurs with bleeding of ectopic endometrium in the
rectosigmoid musculature and fibrosis.
Endometriosis
 Complication
• Infertility results from
– Adhesions pulling uterus out of normal
position
– Blockage of fallopian tubes
 Nursing Diagnosis
1. Acute pain r/t to inflammation and adhesions
of endometrial tissue.

2. Deficient knowledge (disease and treatment

options) r/t lack of exposure to information
(PID)
 Pelvic Inflammatory Disease (PID)
• Common infection of reproductive tract
– Particularly fallopian tubes and ovaries
• Includes:
– Cervicitis (cervix)
– Endometritis (uterus)
– Salpingitis (fallopian tubes)
– Oophoritis (ovaries)
• Infection either cute or chronic
• Short-term concerns: peritonitis, pelvic abscess
• Long-term concerns: infertility, high risk of ectopic
pregnancy
 PID—Etiology
• Arise from sexually transmitted diseases
– Gonorrhea
– Chlamydiosis
• Prior episodes of vaginitis or cervicitis precedes
development
• Infection acute during or after menses
– Endometrium more vulnerable
• Can also result from IUD or other contaminated
instrument
– Can perforate wall and lead to inflammation
and infection
 PID—Pathophysiology
• Usually originates as vaginitis or cervicitis
– Often involves several causative bacteria
• Uterus  fallopian tube
– Edema, fills w/ purulent exudate
• Obstructs tube and restricts drainage into uterus
• Exudate drips out of fimbriae onto ovaries and surrounding
tissue
– Peritoneal membrane attempts to localize but peritonitis may
develop
» Abscesses may form; life-threatening
» Cause septic shock
• Adhesions affect tubes and ovaries
– Lead to infertility and ectopic pregnancies
PID
 PID—Signs and Symptoms
• Lower abdominal pain (1st indication)
– Sudden and severe or gradually increasing in
intensity
• Tenderness during pelvic exams
• Purulent discharge at cervix
• Dysuria
• Fever and leukocytosis can occur
– Depends on causative organism
 Nursing Diagnosis
• Acute pain related to stimulation of free
nerve ending 2 to inflammation.

Post op
• Risk for infection related to inadequate
primary defenses
 Age and Health Environment Stress

H-P-G Axis Extrahypothamamic

Nervous System

Hypothalamus

Gonadotropin-releasing
hormone (GnRh)

Anterior Pituitary

Gonadotropins: FSH and LH

Gonads: Ovaries or Testes

Feedback Sex hormones: Inhibin, Feedback

Mechanism Activin, Follistatin Mechanism
Development of Ovarian Follicle
If fertilization occurs, the corpus luteum
enlarges and begin to secretes hormones that
maintain and support pregnancy.

If fertilization does not occur, the corpus luteum

secretes hormones for approx 14 days and then
degenerate, which triggers the maturation of
another follicles.
 Polycystic Ovarian Syndrome
• PCOS is a misnomer because there is
absence of large cyst.
- (>20 mm in diameter) because anovulation.
• Defined as the presence of
any of the two of the following:
polycystic ovary(small cysts)
Oligo-anovulation(few ovulatory cycles)
Hyperandrogenism
 Polycystic Ovarian Syndrome
• Heterogenous condition
characterized by
– LH hypersecretion
– Ovarian hyperandrogenism
– Hyperinsulinemia
– Reduced fertility

• Metabolic and reproductive endocrine

disorder
Common names and confused with…
• Stein-Leventhal Syndrome
• Polycystic ovary disease
• Functional ovarian hyperandrogenism
• Hyperandrogenic chronic anovulation
• Ovarian dysmetabolic syndrome
• Polycystic ovarian syndrome
 Insulin Resistance and Hyperinsulinemia in PCOS

Hyperinsulinemia

↓ SHBG ↑ Ovarian Disorganized

Production androgens ↑ LH/FSH
release

Hyperandrogenism Anovulation

Polycystic Ovary
Syndrome
Clinical Manifestations of PCOS
• Obesity
• Menstrual disturbance
• Oligomenorrhea
• Amenorrhea
• Hyperandrogenism
• Infertility
 Complications
• Dyslipidemia- ↑ LDL, ↓ HDL, ↑triglycerides
• Diabetes Mellitus- 30% of women with or
without obesity will develop type 2 DM by
age 30.
• Cardiovascular Disease; HPN
• Endometrial carcinoma- anovulatory
women are hyperestrogenic
 How to Diagnose PCOS
 Evidence of androgen excess.
 Chronic anovulation.
 Inappropriate Gonadotropin secretion.
 Types of Ovarian Cysts
• Follicular cysts
- dominant follicle fails to rupture or non-
dominant follicles fails to regress.
– pelvic pain, sensation of feeling bloated, irregular menses.
– after several cycles in which the hormone follow regular cycle
and progesterone levels are restored, cysts will absorbed or
regress.
• Research indicates that when progesterone is not being
produced, the hypothalamus releases GnRH to increase
FSH level. FSH continue to stimulates follicular size
and causes follicular cyst to develop.
 Types of Ovarian Cysts
• Corpus Luteum cysts
– affected cysts consist of blood.
– intracystic hemorrhage that can occur in the
vascularization stage
• May become large enough to cause discomfort,
urinary retention, or menstrual irregularities
– Bleeding if ruptures
 Types of Ovarian Cysts
• Dermoid Cysts
– contain elements of all three germ layers.
– these growths may contain skin, hair, sebaceous,
sweat glands, muscle fibers, cartilage and bone.
• Cause even more serious inflammation
– Risk of torsion of the ovary

• Ultrasound and laparoscopy to cyst

 Clinical Signs: Anything
• Oligomenorrhea or Amenorrhea

• Anovulation

• Elevated Androgens

• Enlarged ovaries

• Hyperinsulinemic Insulin Resistance

• Dermatologic abnormalities

• Obesity

• Chronic pelvic pain

Ovarian Cysts
 Physical Examination
• Vaginal ultrasound

• Cysts
– 2-8 millimeter diameter
– Often a “string of pearls”
– Enlarged ovary

• Thickened endometrium
– Lack of menses
 PCOS: Diagnostic Criteria
• Two of three clinical features
– Oligo- or anovulation
– Clinical or biochemical signs of
hyperandrogenism
– Polycystic ovaries on u/s w/o other etiologies
 Blood Test Diagnosis
• ↑ Testosterone
• ↑ DHEA
• ↑ Androstenedione
• ↑ Prolactin
• ↓ Progesterone

• LH:FSH
– 3:1 instead of 1:1
 Laparoscopic Ovarian Drilling
Lasers burn holes in
enlarged follicles

Stimulates ovulation
by reducing LH and
androgen hormones
 Surgery Complications
• Scar tissue

• Lasts a few months

• 80% ovulation rate

• 50% pregnancy rate

• Only used if failed

previous treatments
 Nursing Diagnosis
• Acute pain r/t stimulation of free nerve
ending 2 to adhesion/compression
adjacent organ

• Mild Anxiety r/t performance of invasive

procedure (laparoscopy)
 Breast Cancer—Etiology
• Major cause of death in women
• Incidence continues to increase after age of 20
• Strong genetic predisposition
– identification of specific genes related to cancer
• Hormones also a factor
– Specifically exposure to high estrogen levels
• Long period of regular menstrual cycles (early menarche to
late menopause)
• No kids (nulliparily)
• Delay of 1st pregnancy
– Role of exogenous estrogen (birth control pills,
supplements) still controversial
 Factors that influence cancer
development
• Environmental factors
– Chemical carcinogen:
• Chemical, drugs, tobacco
– Physical carcinogen
• ionizing radiation (diagnostic therapeutic x
ray)
• Ultraviolet light radiation (sun, tanning
beds, germicidal lights), chronic irritation
and tissue trauma.
Factors that influence cancer
development
• Environmental factors
– Viral carcinogen: virus capable of causing
cancer are known as oncovirus (EBV, HBV,
HPV)

• Dietary factors
– High fat, low fiber diet; high in animal fat
intake, preservatives, additives, and nitrate C.
Factors that influence cancer
development
• Genetic predisposition
– factors include an inheritance predisposition to
specific cancers, familial clustering and chromosomal
abberations.
• Age: Advancing age is the most significant risk factor for
cancer development.
• Immune function
– Higher in immunosupressed individual, organ
transplant recipient who are taking immunosupressive
medication, individual with
AIDS.
 Malignant Tumors: Carcinoma of the
Breast—Pathophysiology
• Develop in upper outer quadrant of breast in ½ of
the cases
• Central portion of the breast is also common
• Most tumors are unilateral
• Different types; majority arise from ductal
epithelium
– Infiltrates surrounding tissue and adheres to skin
• Causes dimpling
• Tumor becomes fixed when adheres to muscle or fascia of chest
wall
 Carcinoma of the Breast—
Pathophysiology
• Malignant cells spread at early state
– 1st to close lymph nodes
• Axillary nodes
– In most cases, several nodes infected at time of diagnosis
• metastasizes quickly to lungs, brain, bone, liver
• Tumor cells graded on basis of degree of differentiation
or anaplasia
– Tumor then staged based on size of primary tumor, # lymph
nodes, presence of metastases
• Presence of estrogen and progesterone receptors
– Major factor in determining how to treat the pt’s cancer
Breast Cancer
 Breast Cancer—Signs and
Symptoms
• Initial sign is single, hard, painless nodule
– Mass is freely movable in early stage
• Becomes fixed
• Advanced signs
– Fixed nodule
– Dimpling of skin
– Discharge from nipple
– Change in breast contour
• Biopsy confirms diagnosis of malignancy
 General Warning Signs of Cancer

• C hange in bowel or bladder habits

• A ny sores that does not heal
• U nusual bleeding or discharge.
• T hickening or lump in breast or elsewhere
• I ndigestion
• O bvious change in wart or mole
• N agging cough or hoarseness
 Grading
• Grade I – cells differ slightly from normal cells
and are more differentiated (mild dysplasia)
• Grade II- cells are more abnormal and are
moderately differentiated (moderate dysplasia)
• Grade III – cells are very abnormal and are
poorly differentiated (severe dysplasia)
• Grade IV – cells are immature (anaplasia) and
undifferentiated; cells of origin are difficult to
determine.
 Staging
• Stage O: Carcinoma in situ (histologic char. of
malignancy)
• Stage I: Tumor limited to tissue if origin;
localized growth of tumor.
• Stage II: Limited local spread.
• Stage III: extensive local and regional spread.
• Stage IV: Metastasis
 Complications
• Bone cancer.
• Lung cancer
 Nursing Diagnosis
• Disturbed body image r/t removal of breast.
• Fatigue related to effects of disease and
treatments
• Impaired skin integrity related to incision
following breast surgery
• Ineffective sexuality patterns related to
perceived loss of attractiveness after
mastectomy
 Diagnostic
Biopsy – definitive means of diagnosing cancer
and provides histological proof of malignancy.
Types:
Needle: aspiration of cells
Incisional: removal of wedge of suspected
tissue from larger mass.
Excisional: Complete removal of the entire
tissue.
Diagnostic
Tissue examination
Frozen section
- diagnosis can be made only minutes are required
for this test.
Paraffin section
- takes about 24 hours for the result.
- It provides a clearer details than those of frozen
section.
 THE END

Section A & B Quizzes Schedule

• Sept 22 (wed) CNS

• Sept 23 (thu) Muscu 6:45 am – 7: 30 am
• Sept 24 (fri) Repro
 Sked of Quizzes (Sec C&D)

Sept. 17 CNS Alteration- 9 to 10 am.

Sept 27, 2010 Musculoskeletal & Repro -
6pm -8 pm